In the neurology literature it is widely known that central nervous system damage can produce forms of psychopathology (e.g., depression, "denial" of illness, acquired psychopathy) that are virtually indistinguishable from their "functional" psychiatric counterparts. The overall focus of our research is to use an ablative paradigm in order to learn more about the role of cortical sites in the affective modulation of behavior. Recent evidence from humans suggests that startle eyeblinks are enhanced during negative affective states and reduced during positive affect. Although animal studies have targeted the amygdala as a key structure in fear potentiated startle and anxiety states, lesions at some cortical sites that relay information to the amygdala appear to attenuate fear potentiated startle in rodents of completely eliminate them following others. No human data currently exist concerning which cortical sites might contribute to affect modulation of startle, or whether hemispheric asymmetries might exist. This is the focus of the investigator's present research. In the proposed studies, the investigator wishes to extend her ongoing funded research in humans with amygdala damage to more broadly encompass individuals with cortical lesions that interact prominently with the amygdala. She hypothesizes that disruption of those cortical systems (e.g., orbitofrontal) that are most closely linked with amygdala will dramatically alter valence modulation of startle and other aspects of emotional behavior. To address this hypothesis, patients with discrete lesions involving orbitofrontal, dorsolateral frontal, or posterior temporal sites within the right or left hemisphere will be evaluated. Eyeblink startle responses will be elicited while subjects concurrently engage in affect eliciting tasks (shock induced anticipatory anxiety, viewing emotional scenes, listening to affective sounds). During these tasks, multiple measures of emotional reactivity will be obtained including verbal report and psychophysiologic measures sensitive to arousal (skin conductance), valence (startle eyeblink, facial EMG), and processing demands. As designed, she hopes to learn whether: a) there is differential decoupling among these emotion response systems due to integrity of particular cortical sites; b) whether valence modulation of the startle response is differently affected by lesions involving frontal or posterior temporal sites; c) whether obtained patterns of findings are more consistent with one of several neuropsychological laterality models of emotion processing (bivalent, right hemisphere, etc.). Hopefully, the obtained data will provide useful information about emotional disorders and psychopathology that occur following dysfunction of specific neural systems within the brain.